ABSTRACT
Background@#and Purpose To evaluate whether the thrombus enhancement sign (TES) can be used to differentiate embolic large vessel occlusion (LVO) from in situ intracranial atherosclerotic stenosis (ICAS)-related LVO in the anterior circulation of patients with acute ischemic stroke (AIS). @*Methods@#Patients with LVO in the anterior circulation who underwent both non-contrast computed tomography (CT) and CT angiography and mechanical thrombectomy were retrospectively enrolled. Both embolic LVO (embo-LVO) and in situ ICAS-related LVO (ICAS-LVO) were confirmed by two neurointerventional radiologists after reviewing the medical and imaging data. TES was assessed to predict embo-LVO or ICAS-LVO. The associations between occlusion type and TES, along with clinical and interventional parameters, were investigated using logistic regression analysis and a receiver operating characteristic curve. @*Results@#A total of 288 patients with AIS were included and divided into an embo-LVO group (n=235) and an ICAS-LVO group (n=53). TES was identified in 205 (71.2%) patients and was more frequently observed in those with embo-LVO, with a sensitivity of 83.8%, specificity of 84.9%, and area under the curve (AUC) of 0.844. Multivariate analysis showed that TES (odds ratio [OR], 22.2; 95% confidence interval [CI], 9.4–53.8; P<0.001) and atrial fibrillation (OR, 6.6; 95% CI, 2.8–15.8; P<0.001) were independent predictors of embolic occlusion. A predictive model that included both TES and atrial fibrillation yielded a higher diagnostic ability for embo-LVO, with an AUC of 0.899. @*Conclusion@#TES is an imaging marker with high predictive value for identifying embo- and ICAS-LVO in AIS and provides guidance for endovascular reperfusion therapy.
ABSTRACT
Objective To construct pEGFP-C2-AQP4-M23 plasmid and to detect its expression in CTX-TNA2 cells in order to study the effect of AQP4 on astrocytes in hypoglycemia. Methods AQP4 gene obtained from SD rats by RT-PCR was cloned into pEGFP-C2 plasmid. The recombinant plasmid was transfected into CTX-TNA2 cells, then treated with low glucose. The expression and effect of AQP4 on CTX-TNA2 cells were examed with confocol. Results PCR and enzyme digestion showed AQP4 size was right; confocol demonstrated that AQP4 was expressed on the membrane of CTX-TNA2 cells, and the surfacial area of CTX-TNA2 cells with AQP4was larger than those without AQP4 in hypoglycemia. Conclusion pEGFP-C2-AQP4-M23 plasmid was successfully constructed and expressed in the CTX-TNA2 cell membrane and AQP4 plays an important role in cell edema in hypoglycemia.